BREAKING BOMBSHELL: What the Next "Pandemic" Will Look Like

“That, you know, I’d say— ah— will get attention this time.”

— Bill Gates

The democidal maniacs are ramping up their followup COVID-19 fear-mongering, but that will merely serve as their ingenious head fake.

The next “pandemic” will be one that scant few are expecting, with the requisite brand new Modified mRNA DEATHVAX™ offerings.

The PSYOP-23 Followup

This upcoming outbreak will be the Nipah virus, which is yet another lab created bioweapon brought to us courtesy of the Gain of Function all-star team of Fauci, Gates, NIH, CIA, DoD, Pentagon, CFR, UN, WHO, WEF, Rockefeller Foundation, the Wuhan Institute of Virology, et al.

According to a research study from 2021 entitled, Nipah virus vector sequences in COVID-19 patient samples sequenced by the Wuhan Institute of Virology, the latest franken-virus was sequenced at the very same lab that released C-19:

We report the detection of Nipah virus in an infectious clone format, a BSL4-level pathogen and CDC-designated Bioterrorism Agent, in raw RNA-Seq sequencing reads deposited by the Wuhan Institute of Virology (WIV) produced from five December 2019 patients infected with SARS-CoV-2. Research involving Nipah infectious clones has never been reported to have occured at the WIV. These patient samples have been previously reported to contain reads from several other viruses: Influenza A, Spodoptera frugiperda rhabdovirus and Nipah. Previous authors have interpreted the presence of these virus sequences as indicative of co-infections of the patients in question by these pathogens or laboratory contamination. However, our analysis shows that NiV genes are encapsulated in synthetic vectors, which we infer was for assembly of a NiV infectious clone. In particular, we document the finding of internal N, P-V-W-C and L protein coding sequences as well as coverage of the G and F genes. Furthermore, the format of Hepatitis D virus ribozyme and T7 terminator downstream of the 5-prime end of the NiV sequence is consistent with truncation required at the end of the genome for a full length infectious clone. This indicates that research at WIV was being conducted on an assembled NiV infectious clone. Contamination of patient sequencing reads by an infectious NiV clone of the highly pathogenic Bangladesh strain could indicate a significant breach of BSL-4 protocols. We call on WIV to explain the purpose of this research on infectious clones of Nipah Virus, the full chronology of this work, and to explain how and at what stage of sample preparation this contamination occurred.

Mockingbird MSM Seeding

According to the Wall Street Journal, Indian Officials Rush to Contain Outbreak of Deadly Nipah Virus:

Authorities in southern India have ramped up testing and contact tracing for the Nipah virus following two deaths. Health experts said the virus is less contagious than Covid, but has a higher fatality rate.

Additional MSM doom hype came courtesy of a Forbes article last week entitled, What To Know About The Deadly Nipah Virus As India Races To Contain Outbreak:

Health officials in India’s southern state of Kerala are rushing to track and contain an outbreak of Nipah that has already killed two people and hospitalized three others. According to news reports, public health workers have tested hundreds of workers and schools, government buildings, religious institutions, public transport and public offices have been closed or suspended in at-risk areas to curb potential spread. It is the state’s fourth outbreak since 2018 and experts warn the area might be at particular risk from virus spillovers given the destruction of natural bat habitats by humans in the region.

NPR was told to write an article entitled, Another Nipah outbreak in India: What do we know about this virus and how to stop it?:

"The virus has an incubation period of 14-21 days," says Anish. "Judging from the time of the secondary infections, we're still in the middle of this outbreak," he says. And there's at least one piece of the puzzle that authorities still don't know — How the patient Ali contracted Nipah in the first place.

Staggered Staged Multi-Deployments

What this means is that the Nipah virus has a higher rapid kill rate, or IFR (infection fatality rate), but will evolve far more quickly into a relatively benign virus; therefore, this “pandemic” will require sustained populace-wide aerosolized pulses, or deployments.

In other words, Nipah will have a slow build across “random” populations, exact quick death tolls, with staggered additional pulses across other seemingly random regions, and then reintroduced pulses concurrent with more new regional deployments to create the impression of a “sustained” and “worsening” global “outbreak.”

School Vector

This time the most effective “epidemic” vector will occur in schools, where traditionally non-existent IFR levels of immunologically robust children will be exploited to maximize the fear narrative; to wit:

We also now know that BigPharma on behest of their Intelligence Industrial Complex handlers has been busy developing these complimentary Nipah “vaccines” since last year.

On July 11, 2022, Moderna and the National Institute of Allergy and Infectious Diseases (NIAID) began a clinical trial (NCT05398796) on a new mRNA vaccine for the Nipah Virus.

Now, a little over 1 year later, the media is ramping up their scare tactics for the Nipah virus, a virus that was identified 24 years ago (1999), and has caused isolated outbreaks in Africa and Asia.

Why did they feel it necessary to ramp up a clinical trial 1 year ago for a virus that has killed less than 200 people over the last 24 years, and that has been around since 1947?

Additional Nipah DEATHVAX™ Receipts

NIH launches clinical trial of mRNA Nipah virus vaccine

Dose Escalation, Open-Label Clinical Trial to Evaluate Safety, Tolerability and Immunogenicity of a Nipah Virus (NiV) mRNA Vaccine, mRNA-1215, in Healthy Adults

Never-Ending Simulations

And just like the tabletop and simulation exercises EVENT 201 and DARK WINTER, the same criminal players have been hard at work game planning the imminent Nipah “pandemic.”

In 2019 Johns Hopkins ran a tabletop exercise called CLADE X which references the Nipah virus:

The purpose of the exercise was to illustrate high-level strategic decisions and policies that the United States and the world will need to pursue in order to prevent a pandemic or diminish its consequences should prevention fail.

On March 14, 2022, four months before the clinical trial, The Gates Foundation announced a new $90 million funding initiative named Pandemic Antiviral Discovery (PAD):

Novo Nordisk Foundation, Open Philanthropy, and Bill & Melinda Gates Foundation Launch Initiative to Support New Antiviral Medicines for Future Pandemics

The focus of the first RFP will be henipavirus, a subfamily of paramyxovirus that includes Nipah virus—a pathogen with an estimated fatality rate of 40% to 75%.

Clearly, “Gates” is the most prescient man in the world when it comes to viral outbreaks and “vaccines;” except that we have incontrovertible proof as per the above 2021 research study that Nipah is a bioweapon.

Comparing Nipah virus to SARS-CoV-2, we know that both are enveloped, single-stranded RNA viruses that can cause severe respiratory illness in humans; however, they belong to different families: Nipah is a paramyxovirus, while SARS-CoV-2 is a coronavirus.

Nipah Virus and SARS-CoV-2 Similarities and Pertinent Features:

Cell Entry

Nipah virus enters cells through ephrin-B2 and ephrin-B3 receptors.

SARS-CoV-2 uses the ACE2 receptor for cell entry and requires priming by the TMPRSS2 protease.

Furin Cleavage Site

Nipah virus’ fusion (F) protein is processed by furin during its biogenesis in the host cell.

SARS-CoV-2’s spike protein contains a unique insertion, which has a furin-like cleavage site that enhances its binding to human cells.

Cellular Mechanisms and Intracellular pH

Viruses often manipulate intracellular pathways, including those that regulate pH, to facilitate their replication and assembly; for example, some enveloped viruses, including coronaviruses, require low pH for fusion with the endosome once they enter the cell.

The strategy of raising cellular pH to inhibit viral replication has been explored for various viruses, including SARS-CoV-2. Ivermectin and Fenbendazole  are known to raise endosomal pH, and have been studied in the context of SARS-CoV-2.

Protein Assembly

Both viruses replicate and assemble in the cytoplasm of the infected cell.

Glycosylation

Glycosylation is a common post-translational modification for many viral proteins. It can affect protein folding, stability, and interactions with host immunity.

Nipah virus’ G (attachment) and F (fusion) proteins of Nipah are also glycosylated.

SARS-CoV-2’s spike protein is heavily glycosylated, which is believed to help the virus evade the immune system.

Potential Mechanism of Spread Inhibition

As mentioned earlier, interfering with pH regulation, targeting cellular proteases like furin and TMPRSS2, and blocking the receptors or their interaction with viral proteins are all potential strategies to inhibit viral entry and spread.

In other words, a combination therapy of Fenbendazole and Ivermectin may be the most effective strategy for the prevention and treatment of the Nipah virus.

Nipah Virus Compared to Ebola

The Nipah virus and the Ebola virus are both RNA viruses that cause severe and often fatal illness in humans, but they belong to different families and have distinct genomic and biological properties; however, they do share some similarities in their mechanisms of cellular entry and intracellular transport:

Ephrin Receptors

Nipah virus uses ephrin-B2 and ephrin-B3 as entry receptors.

Ebola Virus utilizes the ephrin-B2 receptor for entry into endothelial cells.

Intracellular Transport

Both viruses utilize the cellular cytoskeleton for transport, though the specifics might differ.

The exact mechanisms and proteins involved in the intracellular transport of Nipah virus are less well-characterized compared to Ebola, but microtubules and other cytoskeletal components likely play a role.

The VP40 protein of Ebola is better understood, having been shown to interact with the cellular protein NEDD4, which facilitates budding and release of the virus particles from the host cell. This process involves components of the cellular cytoskeleton.

Pathogenesis and Immune Evasion

Both viruses have mechanisms for evading the host's immune response, leading to unchecked replication and severe disease.

The V and W proteins of Nipah virus interfere with host interferon signaling.

The VP24 protein of Ebola inhibits interferon signaling in the host cell.

Clinical Manifestations

Both viruses can cause severe hemorrhagic fever in humans, characterized by fever, organ dysfunction, and bleeding. However, the clinical manifestations and progression can vary.

In Conclusion

The best protocol for the Nipah virus uses both the SARS-CoV-2 and Ebola/Marburg courses of treatment in a combination of Fenbendazol, Ivermectin and Doxycycline.

Doxycycline is an important drug because it prevents and treats cytokine storms, while inhibiting the Matrix metalloproteases (MMP) enzyme that catalyzes tissue injury and scarring. This is also important when dealing with “vaccine” spike protein, or SP 2-induced myocarditis as Doxycycline attenuates the heart scarring, thus protecting the heart from indefinite SP 2 scarring.

It is no wonder that governments actively discourage the use of Doxycycline in treating SARS-CoV-2 patients despite the overwhelming evidence of its importance.

This Substack will soon be publishing an in-depth article on Doxycycline as a critical component of not just SARS-CoV-2 therapy, but Nipah, Ebola/Marburg, as well as turbo cancers.

And now that we know what the next “pandemic” is going to be, your attention may now be focused on the fact that we know exactly how to deal with it.

Do NOT fear.

Good always defeats evil.

And NEVER comply.

References:

Negrete OA, et al. EphrinB2 is the entry receptor for Nipah virus, an emergent deadly paramyxovirus. Nature. 2005.

Hoffmann M, et al. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020.

Coutard B, et al. The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade. Antiviral Research. 2020.

Diederich S, et al. Activation of the Nipah virus fusion protein in MDCK cells is mediated by cathepsin B within the endosome-recycling compartment. Journal of Virology. 2008.

Wang M, et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro. Cell Research. 2020.

Watanabe Y, et al. Site-specific glycan analysis of the SARS-CoV-2 spike. Science. 2020.

Pager CT, Dutch RE. Cathepsin L is involved in proteolytic processing of the Hendra virus fusion protein. Journal of Virology. 2005.

Kondratowicz AS, et al. T-cell immunoglobulin and mucin domain 1 (TIM-1) is a receptor for Zaire Ebolavirus and Lake Victoria Marburgvirus. Proceedings of the National Academy of Sciences. 2011.

Harty RN, et al. A PPxY motif within the VP40 protein of Ebola virus interacts physically and functionally with a ubiquitin ligase: implications for filovirus budding. Proceedings of the National Academy of Sciences. 2000.

Reid SP, et al. Ebola virus VP24 binds karyopherin alpha1 and blocks STAT1 nuclear accumulation. Journal of Virology. 2006.

Rodriguez JJ, et al. Paramyxovirus V proteins disrupt the fold of the RNA sensor MDA5 to inhibit antiviral signaling. Science. 2013.